We have proposed that critical changes in the redox state of the beta cell may be involved in the pathogenesis of chemically induced diabetes, while small changes in the redox state may modify insulin release. In vitro studies indicate that toxic doses of the chemical diabetogenic agents, streptozotocin and alloxan, act as oxidants and cause a change in the redox state of the cell. This is demonstrated by a fall in the ratio of the reduced to oxidized glutathione in red blood cells and in islets. These agents also enhance the activity of the hexose monophosphate shunt in islets. Furthermore, in rats, the antioxidant alpha tocopherol, exerts a protective effect against the diabetogenic effect of streptozotocin and alloxan. Whereas rats on an alpha tocopherol and selenium depleted diet, become diabetic on a non-toxic dose of streptozotocin. Very low concentrations of alloxan cause small changes in the redox state of islets, which are coincident with the first phase of insulin release. Further studies on the relationship of alloxan and streptozotocin to insulin release are underway. The acute metabolic events following EMC virus-induced diabetes in mice and the possible effect of this virus on the redox state of islets, are to be investigated.